1
40
15
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.jep.2020.112660" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jep.2020.112660</a>
Pages
112660-112660
Volume
253
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.jep.2020.112660" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.jep.2020.112660</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Update Year & Number
March 2020 Update
NEOMED College
NEOMED College of Pharmacy
NEOMED Department
Department of Pharmaceutical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Songling Xuemaikang Capsule inhibits isoproterenol-induced cardiac hypertrophy via CaMKIIdelta and ERK1/2 pathways.
Publisher
An entity responsible for making the resource available
Journal of ethnopharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-02
Subject
The topic of the resource
ERK1/2; Cardiac hypertrophy; Isoproterenol; CaMKIIdelta; Songling xuemaikang capsule; CaMKIIδ
Creator
An entity primarily responsible for making the resource
Qi Jianyong; Tan Yafang; Fan Dancai; Pan Wenjun; Yu Juan; Xu Wen; Wu Jiashin; Zhang Minzhou
Description
An account of the resource
ETHNOPHARMACOLOGICAL RELEVANCE: Cardiac hypertrophy is a key pathologic process in heart failure. Songling Xuemaikang Capsule (SXC), is a formulae of Chinese Medicine commonly used in China to treat hypertension and heart failure. However, its mechanism of effects on cardiac hypertrophy is still unclear. AIM OF THE STUDY: The aims of the present study were to investigate the cardio-protection roles and detailed mechanisms of SXC on cardiac hypertrophy in vivo and in vitro. MATERIALS AND METHODS: A rat model of cardiac hypertrophy was constructed by isoproterenol (ISO) intraperitoneal injection (i.p), 10 mg/kg/day for 3 days, and 4 groups were compared: CON (n = 8), ISO (n = 8), MET (metoprolol, positive drug treatment, n = 7), and SXC (SXC treatment, n = 6). Cardiac structure and function were evaluated with echocardiography in vivo. Dose-dependent curve was obtained with SXC different concentrations. In addition, H9C2 rat cardiomyocytes were cultured in vitro and the phosphorylation of ERK1/2, p38, JNK, AKT, and protein expression of CaN, CaMKIIdelta, GATA4 were detected with Western blot test. RESULTS: The results showed that SXC reduced diastolic thickness of left ventricular posterior wall, while did not change ejection fraction and fraction shortening significantly (P > 0.05). SXC inhibit ISO-induced cardiac hypertrophy dose-dependently with 50% inhibiting concentration (IC50) is 0.504 g/kg/day. Moreover, SXC inhibited the protein expression of CaMKIIdelta, and the phosphorylation of ERK1/2, so inhibiting protein expression of GATA4 in nucleus, and brain natriuretic peptide in serum (P < 0.001). CONCLUSION: The mechanism of SXC in the treatment of heart diseases involves SXC dose-dependently inhibited the ISO-induced cardiac hypertrophy via inhibiting CaMKIIdelta and ERK1/2/GATA4 signaling pathway.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jep.2020.112660" target="_blank" rel="noreferrer noopener">10.1016/j.jep.2020.112660</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2020
CaMKIIdelta
CaMKIIδ
Cardiac hypertrophy
Department of Pharmaceutical Sciences
ERK1/2
Fan Dancai
isoproterenol
Journal of Ethnopharmacology
NEOMED College of Pharmacy
Pan Wenjun
Qi Jianyong
Songling xuemaikang capsule
Tan Yafang
Wu Jiashin
Xu Wen
Yu Juan
Zhang Minzhou
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1155/2014/769515" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2014/769515</a>
Pages
1–9
Volume
2014
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Apocynum Tablet Protects against Cardiac Hypertrophy via Inhibiting AKT and ERK1/2 Phosphorylation after Pressure Overload.
Publisher
An entity responsible for making the resource available
Evidence-based Complementary & Alternative Medicine (eCAM)
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-01
Subject
The topic of the resource
Mice; Gene Expression Profiling; Signal Transduction; Echocardiography; Staining and Labeling; Descriptive Statistics; Funding Source; Post Hoc Analysis; One-Way Analysis of Variance; T-Tests; Blotting; Western; Animal Studies; In Vivo Studies; Vasoconstriction; Phosphorylation – Drug Effects; Aorta – Physiopathology; Heart Diseases – Prevention and Control; Hypertrophy – Prevention and Control; Plant Extracts – Therapeutic Use; Protein Kinases – Antagonists and Inhibitors
Creator
An entity primarily responsible for making the resource
Qi Jianyong; Liu Qin; Gong Kaizheng; Yu Juan; Wang Lei; Guo Liheng; Zhou Miao; Wu Jiashin; Zhang Minzhou
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2014/769515" target="_blank" rel="noreferrer noopener">10.1155/2014/769515</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Animal Studies
Aorta – Physiopathology
Blotting
Descriptive Statistics
Echocardiography
Evidence-based Complementary & Alternative Medicine (eCAM)
Funding Source
Gene Expression Profiling
Gong Kaizheng
Guo Liheng
Heart Diseases – Prevention and Control
Hypertrophy – Prevention and Control
In Vivo Studies
Liu Qin
Mice
One-Way Analysis of Variance
Phosphorylation – Drug Effects
Plant Extracts – Therapeutic Use
Post Hoc Analysis
Protein Kinases – Antagonists and Inhibitors
Qi Jianyong
Signal Transduction
Staining and Labeling
T-Tests
Vasoconstriction
Wang Lei
Western
Wu Jiashin
Yu Juan
Zhang Minzhou
Zhou Miao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3978/j.issn.2304-3881.2014.12.06" target="_blank" rel="noreferrer noopener">http://doi.org/10.3978/j.issn.2304-3881.2014.12.06</a>
Pages
88–100
Issue
2
Volume
4
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Sirtuin 1 signaling and alcoholic fatty liver disease.
Publisher
An entity responsible for making the resource available
Hepatobiliary surgery and nutrition
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-04
Subject
The topic of the resource
lipid metabolism; inflammation; signal transduction; transcriptional regulators; alcoholic fatty liver; Sirtuin 1 (SIRT1)
Creator
An entity primarily responsible for making the resource
You Min; Jogasuria Alvin; Taylor Charles; Wu Jiashin
Description
An account of the resource
Alcoholic fatty liver disease (AFLD) is one of the most prevalent forms of liver disease worldwide and can progress to inflammation (hepatitis), fibrosis/cirrhosis, and ultimately lead to end stage liver injury. The mechanisms, by which ethanol consumption leads to AFLD, are complicated and multiple, and remain incompletely understood. Nevertheless, understanding its pathogenesis will facilitate the development of effective pharmacological or nutritional therapies for treating human AFLD. Chronic ethanol consumption causes steatosis and inflammation in rodents or humans by disturbing several important hepatic transcriptional regulators, including AMP-activated kinase (AMPK), lipin-1, sterol regulatory element binding protein 1 (SREBP-1), PPARgamma co-activator-1alpha (PGC-1alpha), and nuclear transcription factor-kappaB (NF-kappaB). Remarkably, the effects of ethanol on these regulators are mediated in whole or in part by inhibition of a central signaling molecule, sirtuin 1 (SIRT1), which is a nicotinamide adenine dinucleotide (NAD(+), NADH)-dependent class III protein deacetylase. In recent years, SIRT1 has emerged as a pivotal molecule controlling the pathways of hepatic lipid metabolism, inflammatory responses and in the development of AFLD in rodents and in humans. Ethanol-mediated SIRT1 inhibition suppresses or stimulates the activities of above described transcriptional regulators and co-regulators, thereby deregulating diverse lipid metabolism and inflammatory response pathways including lipogenesis, fatty acid beta-oxidation, lipoprotein uptake and secretion and expression of pro-inflammatory cytokines in the liver. This review aims to highlight our current understanding of SIRT1 regulatory mechanisms and its response to ethanol-induced toxicity, thus, affirming significant role of SIRT1 signaling in the development of AFLD.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3978/j.issn.2304-3881.2014.12.06" target="_blank" rel="noreferrer noopener">10.3978/j.issn.2304-3881.2014.12.06</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
alcoholic fatty liver
Department of Pharmaceutical Sciences
Hepatobiliary surgery and nutrition
Inflammation
Jogasuria Alvin
Lipid Metabolism
NEOMED College of Pharmacy
Signal Transduction
Sirtuin 1 (SIRT1)
Taylor Charles
transcriptional regulators
Wu Jiashin
You Min
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.2174/1874467208666150817112109" target="_blank" rel="noreferrer noopener">http://doi.org/10.2174/1874467208666150817112109</a>
Pages
226–236
Issue
3
Volume
10
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Signal Transduction Mechanisms of Alcoholic Fatty Liver Disease: Emer ging Role of Lipin-1.
Publisher
An entity responsible for making the resource available
Current molecular pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-7
Subject
The topic of the resource
Humans; Animals; AMP-Activated Protein Kinases/metabolism; Signal Transduction; Lipid Metabolism; Fatty Liver; Liver/metabolism; lipid metabolism; alcoholic fatty liver disease; inflammation; Lipin-1; signal transduction; transcriptional regulators; Phosphatidate Phosphatase/*metabolism; Inflammation/metabolism; Ethanol/chemistry/*metabolism; Sirtuin 1/metabolism; Alcoholic/*metabolism/pathology
Creator
An entity primarily responsible for making the resource
You Min; Jogasuria Alvin; Lee Kwangwon; Wu Jiashin; Zhang Yanqiao; Lee Yoon-Kwang; Sadana Prabodh
Description
An account of the resource
Lipin-1, a mammalian phosphatidic acid phosphatase (PAP), is a bi-functional molecule involved in various signaling pathways via its function as a PAP enzyme in the triglyceride synthesis pathway and in the nucleus as a transcriptional co-regulator. In the liver, lipin-1 is known to play a vital role in controlling the lipid metabolism and inflammation process at multiple regulatory levels. Alcoholic fatty liver disease (AFLD) is one of the earliest forms of liver injury and approximately 8-20% of patients with simple steatosis can develop into more severe forms of liver injury, including steatohepatitis, fibrosis/ cirrhosis, and eventually hepatocellular carcinoma (HCC). The signal transduction mechanisms for alcohol-induced detrimental effects in liver involves alteration of complex and multiple signaling pathways largely governed by a central and upstream signaling system, namely, sirtuin 1 (SIRT1)-AMP activated kinase (AMPK) axis. Emerging evidence suggests a pivotal role of lipin-1 as a crucial downstream regulator of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.2174/1874467208666150817112109" target="_blank" rel="noreferrer noopener">10.2174/1874467208666150817112109</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
alcoholic fatty liver disease
Alcoholic/*metabolism/pathology
AMP-Activated Protein Kinases/metabolism
Animals
Current molecular pharmacology
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Ethanol/chemistry/*metabolism
Fatty Liver
Humans
Inflammation
Inflammation/metabolism
Jogasuria Alvin
Lee Kwangwon
Lee Yoon-Kwang
Lipid Metabolism
Lipin-1
Liver/metabolism
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED College of Pharmacy
Phosphatidate Phosphatase/*metabolism
Sadana Prabodh
Signal Transduction
Sirtuin 1/metabolism
transcriptional regulators
Wu Jiashin
You Min
Zhang Yanqiao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.18632/oncotarget.22440" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/oncotarget.22440</a>
Pages
108958–108969
Issue
65
Volume
8
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Shexiang Tongxin dropping pill protects against isoproterenol-induced myocardial ischemia in vivo and in vitro.
Publisher
An entity responsible for making the resource available
Oncotarget
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Subject
The topic of the resource
isoproterenol; myocardial ischemia; rat; Shexiang Tongxin dropping pill; signaling pathway
Creator
An entity primarily responsible for making the resource
Qi Jianyong; Pan Wenjun; Tan Yafang; Luo Jiaru; Fan Dancai; Yu Juan; Wu Jiashin; Zhang Minzhou
Description
An account of the resource
Shexiang Tongxin dropping pill (STDP) is a formulae of Chinese Medicine commonly used to treating angina pectoris in China. However, its mechanism of action is still yet unclear. This study investigated the roles of STDP on myocardial ischemia injury. We constructed a rat model of myocardial injury (isoproterenol subcutaneous injection, i.h, 85 mg/kg/day for 2 days), and compared among 4 groups: CON (control), ISO (ischemic injury model), MET (metoprolol), and STDP. Serum contents of Troponin I (cTnI), creatine kinase (CK), CK-MB, lactate dehydrogenase (LDH), alpha-hydroxybutyric dehydrogenase (alpha-HBD), and Aspartate Aminotransferase were detected and five STDP doses (1, 10, 100, 1000 and 10000 mg/kg/day) were chosen to obtain a dose-response curve. Western-blot was used to detect phosphorylations of extracellular signal-regulated kinase 1/2 (ERK1/2), protein kinase B (AKT), and camodulin kinase II (CamkII). Furthermore, an ERK1/2 inhibitor PD98059, a phosphatidylinositol-3-kinase inhibitor, LY294002, and a CamKII inhibitor, KN-93 were administered i.h. RESULTS: cTnI, CK, CK-MB, alpha-HBD, and LDH were significantly lower in STDP than ISO (P\textless0.05). STDP exhibited a dose-dependent effect with a half maximal inhibitory concentration of 42 mg/kg/day. Phosphorylation of ERK1/2 was enhanced in the STDP group (vs. ISO, P\textless0.05), while AKT and CamkII were not changed. Further, the protective effects of STDP were offset by PD98059 administration i.h. In conclusion, STDP protected against the ISO-induced myocardial ischemic injury via an ERK1/2 signaling pathway, which provided a mechanism to support clinical applications of STDP as treatment for ischemic heart disease.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.18632/oncotarget.22440" target="_blank" rel="noreferrer noopener">10.18632/oncotarget.22440</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Fan Dancai
isoproterenol
Luo Jiaru
myocardial ischemia
Oncotarget
Pan Wenjun
Qi Jianyong
rat
Shexiang Tongxin dropping pill
signaling pathway
Tan Yafang
Wu Jiashin
Yu Juan
Zhang Minzhou
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1371/journal.pone.0166560" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0166560</a>
Pages
e0166560–e0166560
Issue
11
Volume
11
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Salvianolic Acid B Alleviates Heart Failure by Inactivating ERK1/2/GATA4 Signaling Pathway after Pressure Overload in Mice.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016
Subject
The topic of the resource
Male; Animals; Mice; Phosphorylation/drug effects; Signal Transduction/*drug effects; Rats; Cell Line; Proto-Oncogene Proteins c-akt/metabolism; Benzofurans/chemistry/*pharmacology; Blood Pressure/drug effects; GATA4 Transcription Factor/metabolism; Heart Failure/metabolism/*pathology; Heart Ventricles/diagnostic imaging; Mitogen-Activated Protein Kinase 1/metabolism; Mitogen-Activated Protein Kinase 3/metabolism; Myocardium/metabolism/pathology; Drugs; Inbred C57BL; Animal; Disease Models; Myocytes; Aorta; Brain/blood; Natriuretic Peptide; Cardiac/cytology/drug effects/metabolism; Chinese Herbal/chemistry/pharmacology; Thoracic/surgery
Creator
An entity primarily responsible for making the resource
Yu Juan; Chen Renshan; Tan Yafang; Wu Jiashin; Qi Jianyong; Zhang Minzhou; Gu Weiwang
Description
An account of the resource
BACKGROUND: Heart failure(HF) is a dangerous disease that affects millions of patients. Radix Salvia is widely used in Chinese clinics to treat heart diseases. Salvianolic acid B(SalB) is the major active component of Radix Salvia. This study investigated the mechanisms of action and effects of SalB on HF in an experimental mouse model of HF. METHODS: We created a mouse model of HF by inducing pressure overload with transverse aortic constriction(TAC) surgery for 2 weeks and compared among 4 study groups: SHAM group (n = 10), TAC group (n = 9), TAC+MET group (metprolol, positive drug treatment, n = 9) and TAC+SalB group (SalB, 240 mg*kg-1*day-1, n = 9). Echocardiography was used to evaluate the dynamic changes in cardiac structure and function in vivo. Plasma brain natriuretic peptide (BNP) concentration was detected by Elisa method. In addition, H9C2 rat cardiomyocytes were cultured and Western blot were implemented to evaluate the phosphorylation of ERK1/2, AKT, and protein expression of GATA4. RESULTS: SalB significantly inhibited the phosphorylation of Thr202/Tyr204 sites of ERK1/2, but not Ser473 site of AKT, subsequently inhibited protein expression of GATA4 and plasma BNP(P \textless 0.001), and then inhibited HF at 2 weeks after TAC surgery. CONCLUSIONS: Our data provide a mechanism of inactivating the ERK1/2/GATA4 signaling pathway for SalB inhibition of the TAC-induced HF.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0166560" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0166560</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Animal
Animals
Aorta
Benzofurans/chemistry/*pharmacology
Blood Pressure/drug effects
Brain/blood
Cardiac/cytology/drug effects/metabolism
Cell Line
Chen Renshan
Chinese Herbal/chemistry/pharmacology
Disease Models
Drugs
GATA4 Transcription Factor/metabolism
Gu Weiwang
Heart Failure/metabolism/*pathology
Heart Ventricles/diagnostic imaging
Inbred C57BL
Male
Mice
Mitogen-Activated Protein Kinase 1/metabolism
Mitogen-Activated Protein Kinase 3/metabolism
Myocardium/metabolism/pathology
Myocytes
Natriuretic Peptide
Phosphorylation/drug effects
PloS one
Proto-Oncogene Proteins c-akt/metabolism
Qi Jianyong
Rats
Signal Transduction/*drug effects
Tan Yafang
Thoracic/surgery
Wu Jiashin
Yu Juan
Zhang Minzhou
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCEP.114.001578" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCEP.114.001578</a>
Pages
1181–1188
Issue
6
Volume
7
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Isolation of canine coronary sinus musculature from the atria by radiofrequency catheter ablation prevents induction of atrial fibrillation.
Publisher
An entity responsible for making the resource available
Circulation. Arrhythmia and electrophysiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-12
Subject
The topic of the resource
*Catheter Ablation; Acetylcholine; Action Potentials; Animal; Animal Studies; Animals; Artificial; atrial fibrillation; Atrial Fibrillation – Etiology; Atrial Fibrillation – Physiopathology; Atrial Fibrillation – Prevention and Control; Atrial Fibrillation/etiology/physiopathology/*prevention & control; Biological; Body Surface Potential Mapping; Cardiac Pacing; catheter ablation; Catheter Ablation; coronary sinus; Coronary Sinus/physiopathology/*surgery; Coronary Vessels – Physiopathology; Coronary Vessels – Surgery; Disease Models; Dogs; Heart Atria/physiopathology/surgery; Heart Atrium – Physiopathology; Heart Atrium – Surgery; Male; Models; optical Vm mapping; Time Factors
Creator
An entity primarily responsible for making the resource
Morita Hiroshi; Zipes Douglas P; Morita Shiho T; Wu Jiashin
Description
An account of the resource
BACKGROUND: The junction between the coronary sinus (CS) musculature and both atria contributes to initiation of atrial tachyarrhythmias. The current study investigated the effects of CS isolation from the atria by radiofrequency catheter ablation on the induction and maintenance of atrial fibrillation (AF). METHODS AND RESULTS: Using an optical mapping system, we mapped action potentials at 256 surface sites in 17 isolated and arterially perfused canine atrial tissues containing the entire musculature of the CS, right atrial septum, posterior left atrium, left inferior pulmonary vein, and vein of Marshal. Rapid pacing from each site before and after addition of acetylcholine (0.5 mumol/L) was applied to induce AF. Epicardial radiofrequency catheter ablation at CS-atrial junctions isolated the CS from the atria. Rapid pacing induced sustained AF in all tissues after acetylcholine. Microreentry within the CS drove AF in 88% of preparations. Reentries associated with the vein of Marshall (29%), CS-atrial junctions (53%), right atrium (65%), and pulmonary vein (76%) (frequently with 2-4 simultaneous circuits) were additional drivers of AF. Radiofrequency catheter ablation eliminated AF in 13 tissues before acetylcholine (P\textless0.01) and in 5 tissues after acetylcholine. Radiofrequency catheter ablation also abbreviated the duration of AF in 12 tissues (P\textless0.01). CONCLUSIONS: CS and its musculature developed unstable reentry and AF, which were prevented by isolation of CS musculature from atrial tissue. The results suggest that CS can be a substrate of recurrent AF in patients after pulmonary vein isolation and that CS isolation might help prevent recurrent AF.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCEP.114.001578" target="_blank" rel="noreferrer noopener">10.1161/CIRCEP.114.001578</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Catheter Ablation
2014
Acetylcholine
Action Potentials
Animal
Animal Studies
Animals
Artificial
Atrial fibrillation
Atrial Fibrillation – Etiology
Atrial Fibrillation – Physiopathology
Atrial Fibrillation – Prevention and Control
Atrial Fibrillation/etiology/physiopathology/*prevention & control
Biological
Body Surface Potential Mapping
Cardiac Pacing
Catheter Ablation
Circulation. Arrhythmia and electrophysiology
coronary sinus
Coronary Sinus/physiopathology/*surgery
Coronary Vessels – Physiopathology
Coronary Vessels – Surgery
Disease Models
Dogs
Heart Atria/physiopathology/surgery
Heart Atrium – Physiopathology
Heart Atrium – Surgery
Male
Models
Morita Hiroshi
Morita Shiho T
optical Vm mapping
Time Factors
Wu Jiashin
Zipes Douglas P
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1155/2014/769515" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2014/769515</a>
Pages
769515–769515
Volume
2014
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Apocynum Tablet Protects against Cardiac Hypertrophy via Inhibiting AKT and ERK1/2 Phosphorylation after Pressure Overload.
Publisher
An entity responsible for making the resource available
Evidence-based complementary and alternative medicine : eCAM
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
1905-07
Creator
An entity primarily responsible for making the resource
Qi Jianyong; Liu Qin; Gong Kaizheng; Yu Juan; Wang Lei; Guo Liheng; Zhou Miao; Wu Jiashin; Zhang Minzhou
Description
An account of the resource
Background. Cardiac hypertrophy occurs in many cardiovascular diseases. Apocynum tablet (AT), a traditional Chinese medicine, has been widely used in China to treat patients with hypertension. However, the underlying molecular mechanisms of AT on the hypertension-induced cardiac hypertrophy remain elusive. The current study evaluated the effect and mechanisms of AT on cardiac hypertrophy. Methods. We created a mouse model of cardiac hypertrophy by inducing pressure overload with surgery of transverse aortic constriction (TAC) and then explored the effect of AT on the development of cardiac hypertrophy using 46 mice in 4 study groups (combinations of AT and TAC). In addition, we evaluated the signaling pathway of phosphorylation of ERK1/2, AKT, and protein expression of GATA4 in the cardioprotective effects of AT using Western blot. Results. AT inhibited the phosphorylation of Thr202/Tyr204 sites of ERK1/2, Ser473 site of AKT, and protein expression of GATA4 and significantly inhibited cardiac hypertrophy and cardiac fibrosis at 2 weeks after TAC surgery (P \textless 0.05). Conclusions. We experimentally demonstrated that AT inhibits cardiac hypertrophy via suppressing phosphorylation of ERK1/2 and AKT.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2014/769515" target="_blank" rel="noreferrer noopener">10.1155/2014/769515</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Evidence-based complementary and alternative medicine : eCAM
Gong Kaizheng
Guo Liheng
Liu Qin
Qi Jianyong
Wang Lei
Wu Jiashin
Yu Juan
Zhang Minzhou
Zhou Miao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M116.737015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M116.737015</a>
Pages
22482–22495
Issue
43
Volume
291
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
MitoNEET Deficiency Alleviates Experimental Alcoholic Steatohepatitis in Mice by Stimulating Endocrine Adiponectin-Fgf15 Axis.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-10
Subject
The topic of the resource
*adiponectin; *alcohol; *intestine; *iron; *liver injury; *Signal Transduction; Adiponectin/genetics/*metabolism; Alcoholic/genetics/*metabolism/pathology; Animals; Fatty Liver; Fibroblast Growth Factors/genetics/*metabolism; Humans; Iron-Binding Proteins/metabolism; Knockout; Male; Membrane Proteins/*deficiency/metabolism; Mice; NF-kappa B/genetics/metabolism; Sirtuin 1/genetics/metabolism
Creator
An entity primarily responsible for making the resource
Hu Xudong; Jogasuria Alvin; Wang Jiayou; Kim Chunki; Han Yoonhee; Shen Hong; Wu Jiashin; You Min
Description
An account of the resource
MitoNEET (mNT) (CDGSH iron-sulfur domain-containing protein 1 or CISD1) is an outer mitochondrial membrane protein that donates 2Fe-2S clusters to apo-acceptor proteins. In the present study, using a global mNT knock-out (mNTKO) mouse model, we investigated the in vivo functional role of mNT in the development of alcoholic steatohepatitis. Experimental alcoholic steatohepatitis was achieved by pair feeding wild-type (WT) and mNTKO mice with Lieber-DeCarli ethanol-containing diets for 4 weeks. Strikingly, chronically ethanol-fed mNTKO mice were completely resistant to ethanol-induced steatohepatitis as revealed by dramatically reduced hepatic triglycerides, decreased hepatic cholesterol level, diminished liver inflammatory response, and normalized serum ALT levels. Mechanistic studies demonstrated that ethanol administration to mNTKO mice induced two pivotal endocrine hormones, namely, adipose-derived adiponectin and gut-derived fibroblast growth factor 15 (Fgf15). The elevation in circulating levels of adiponectin and Fgf15 led to normalized hepatic and serum levels of bile acids, limited hepatic accumulation of toxic bile, attenuated inflammation, and amelioration of liver injury in the ethanol-fed mNTKO mice. Other potential mechanisms such as reduced oxidative stress, activated Sirt1 signaling, and diminished NF-kappaB activity also contribute to hepatic improvement in the ethanol-fed mNTKO mice. In conclusion, the present study identified adiponectin and Fgf15 as pivotal adipose-gut-liver metabolic coordinators in mediating the protective action of mNT deficiency against development of alcoholic steatohepatitis in mice. Our findings may help to establish mNT as a novel therapeutic target and pharmacological inhibition of mNT may be beneficial for the prevention and treatment of human alcoholic steatohepatitis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M116.737015" target="_blank" rel="noreferrer noopener">10.1074/jbc.M116.737015</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*adiponectin
*alcohol
*intestine
*iron
*liver injury
*Signal Transduction
2016
Adiponectin/genetics/*metabolism
Alcoholic/genetics/*metabolism/pathology
Animals
Department of Pharmaceutical Sciences
Fatty Liver
Fibroblast Growth Factors/genetics/*metabolism
Han Yoonhee
Hu Xudong
Humans
Iron-Binding Proteins/metabolism
Jogasuria Alvin
Kim Chunki
Knockout
Male
Membrane Proteins/*deficiency/metabolism
Mice
NEOMED College of Pharmacy
NF-kappa B/genetics/metabolism
Shen Hong
Sirtuin 1/genetics/metabolism
The Journal of biological chemistry
Wang Jiayou
Wu Jiashin
You Min
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/srep42843" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/srep42843</a>
Pages
42843–42843
Volume
7
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mechanisms of Chinese Medicine Xinmailong's protection against heart failure in pressure-overloaded mice and cultured cardiomyocytes.
Publisher
An entity responsible for making the resource available
Scientific reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-02
Subject
The topic of the resource
Animal; Animals; Cardiac/cytology/*drug effects/metabolism; Cell Nucleus/metabolism; Cell Survival/drug effects; Cells; Chinese Herbal/*administration & dosage/pharmacology; Constriction; Cultured; Disease Models; Drugs; Echocardiography; GABA Plasma Membrane Transport Proteins/*metabolism; Gene Expression Regulation/drug effects; Glycogen Synthase Kinase 3 beta/metabolism; Heart Failure/etiology/metabolism/physiopathology/*prevention & control; Humans; MAP Kinase Signaling System/drug effects; Mice; Myocytes; Pathologic; Phosphorylation; Proto-Oncogene Proteins c-akt/metabolism; Rats
Creator
An entity primarily responsible for making the resource
Qi Jianyong; Yu Juan; Tan Yafang; Chen Renshan; Xu Wen; Chen Yanfen; Lu Jun; Liu Qin; Wu Jiashin; Gu Weiwang; Zhang Minzhou
Description
An account of the resource
Patients with heart failure (HF) have high mortality and mobility. Xinmailong (XML) injection, a Chinese Medicine, is clinically effective in treating HF. However, the mechanism of XML's effectiveness on HF was unclear, and thus, was the target of the present study. We created a mouse model of pressure-overload-induced HF with transverse aortic constriction (TAC) surgery and compared among 4 study groups: SHAM (n = 10), TAC (n = 12), MET (metoprolol, positive drug treatment, n = 7) and XML (XML treatment, n = 14). Dynamic changes in cardiac structure and function were evaluated with echocardiography in vivo. In addition, H9C2 rat cardiomyocytes were cultured in vitro and the phosphorylation of ERK1/2, AKT, GSK3beta and protein expression of GATA4 in nucleus were detected with Western blot experiment. The results showed that XML reduced diastolic thickness of left ventricular posterior wall, increased ejection fraction and fraction shortening, so as to inhibit HF at 2 weeks after TAC. Moreover, XML inhibited the phosphorylation of ERK1/2, AKT and GSK3beta, subsequently inhibiting protein expression of GATA4 in nucleus (P \textless 0.001). Together, our data demonstrated that XML inhibited the TAC-induced HF via inactivating the ERK1/2, AKT/GSK3beta, and GATA4 signaling pathway.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/srep42843" target="_blank" rel="noreferrer noopener">10.1038/srep42843</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Animal
Animals
Cardiac/cytology/*drug effects/metabolism
Cell Nucleus/metabolism
Cell Survival/drug effects
Cells
Chen Renshan
Chen Yanfen
Chinese Herbal/*administration & dosage/pharmacology
Constriction
Cultured
Disease Models
Drugs
Echocardiography
GABA Plasma Membrane Transport Proteins/*metabolism
Gene Expression Regulation/drug effects
Glycogen Synthase Kinase 3 beta/metabolism
Gu Weiwang
Heart Failure/etiology/metabolism/physiopathology/*prevention & control
Humans
Liu Qin
Lu Jun
MAP Kinase Signaling System/drug effects
Mice
Myocytes
Pathologic
Phosphorylation
Proto-Oncogene Proteins c-akt/metabolism
Qi Jianyong
Rats
Scientific reports
Tan Yafang
Wu Jiashin
Xu Wen
Yu Juan
Zhang Minzhou
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/srep34117" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/srep34117</a>
Pages
34117–34117
Volume
6
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Myeloid Cell-Specific Lipin-1 Deficiency Stimulates Endocrine Adiponectin-FGF15 Axis and Ameliorates Ethanol-Induced Liver Injury in Mice.
Publisher
An entity responsible for making the resource available
Scientific reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-09
Subject
The topic of the resource
Adiponectin/*blood; Alcoholic/blood/*genetics/metabolism; Animal; Animals; Disease Models; Fatty Liver; Fibroblast Growth Factors/*blood; Gene Knockout Techniques; Lipid Metabolism; Male; Mice; Myeloid Cells/*metabolism; NF-kappa B/metabolism; Nuclear Proteins/*deficiency; Organ Specificity; Phosphatidate Phosphatase/*deficiency; Signal Transduction
Creator
An entity primarily responsible for making the resource
Wang Jiayou; Kim Chunki; Jogasuria Alvin; Han Yoonhee; Hu Xudong; Wu Jiashin; Shen Hong; Chrast Roman; Finck Brian N; You Min
Description
An account of the resource
Lipin-1 is a phosphatidate phosphohydrolase (PAP) required for the generation of diacylglycerol during glycerolipid synthesis, and exhibits dual functions in the regulation of lipid metabolism. Lipin-1 has been implicated in the pathogenesis of alcoholic liver disease (ALD). In the present study, we assessed lipin-1 function in myeloid cells in ALD using a myeloid cell-specific lipin-1 knockout (mLipin-1KO) mouse model. Utilizing the Gao-binge ethanol feeding protocol, matched mLipin-1KO mice and littermate loxP control (WT) mice were pair-fed with either an ethanol-containing diet or an ethanol-free diet (control). Surprisingly, deletion of lipin-1 in myeloid cells dramatically attenuated liver inflammatory responses and ameliorated liver injury that would normally occur following the ethanol feeding protocol, but slightly exacerbated the ethanol-induced steatosis in mice. Mechanistically, myeloid cell-specific lipin-1 deficiency concomitantly increased the fat-derived adiponectin and ileum-derived fibroblast growth factor (FGF) 15. In concordance with concerted elevation of circulating adiponectin and FGF15, myeloid cell-specific lipin-1 deficiency diminished hepatic nuclear factor kappa B (NF-kappaB) activity, limited liver inflammatory responses, normalized serum levels of bile acids, and protected mice from liver damage after ethanol challenge. Our novel data demonstrate that myeloid cell-specific deletion of lipin-1 ameliorated inflammation and alcoholic hepatitis in mice via activation of endocrine adiponectin-FGF15 signaling.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/srep34117" target="_blank" rel="noreferrer noopener">10.1038/srep34117</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Adiponectin/*blood
Alcoholic/blood/*genetics/metabolism
Animal
Animals
Chrast Roman
Department of Pharmaceutical Sciences
Disease Models
Fatty Liver
Fibroblast Growth Factors/*blood
Finck Brian N
Gene Knockout Techniques
Han Yoonhee
Hu Xudong
Jogasuria Alvin
Kim Chunki
Lipid Metabolism
Male
Mice
Myeloid Cells/*metabolism
NEOMED College of Pharmacy
NF-kappa B/metabolism
Nuclear Proteins/*deficiency
Organ Specificity
Phosphatidate Phosphatase/*deficiency
Scientific reports
Shen Hong
Signal Transduction
Wang Jiayou
Wu Jiashin
You Min
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.ijcard.2014.07.234" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ijcard.2014.07.234</a>
Pages
e119–121
Issue
3
Volume
176
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
6-year post-PCI follow-up of a 110-year myocardial infarction patient: a case report.
Publisher
An entity responsible for making the resource available
International journal of cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-10
Subject
The topic of the resource
80 and over; Age Factors; Aged; Female; Follow-up; Follow-Up Studies; Humans; Myocardial infarction; Myocardial Infarction/*diagnosis/*surgery; Percutaneous coronary intervention (PCI); Percutaneous Coronary Intervention/*trends
Creator
An entity primarily responsible for making the resource
Qi Jianyong; Ren Yi; Wang Lei; Guo Liheng; Wu Jiashin; Zhang Minzhou
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ijcard.2014.07.234" target="_blank" rel="noreferrer noopener">10.1016/j.ijcard.2014.07.234</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
80 and over
Age Factors
Aged
Female
Follow-up
Follow-Up Studies
Guo Liheng
Humans
International journal of cardiology
myocardial infarction
Myocardial Infarction/*diagnosis/*surgery
Percutaneous coronary intervention (PCI)
Percutaneous Coronary Intervention/*trends
Qi Jianyong
Ren Yi
Wang Lei
Wu Jiashin
Zhang Minzhou
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.ajpath.2018.05.004" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ajpath.2018.05.004</a>
Pages
1807–1819
Issue
8
Volume
188
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Hepatic Knockdown of Splicing Regulator Slu7 Ameliorates Inflammation and Attenuates Liver Injury in Ethanol-Fed Mice.
Publisher
An entity responsible for making the resource available
The American journal of pathology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-08
Creator
An entity primarily responsible for making the resource
Wang Jiayou; Kainrad Noah; Shen Hong; Zhou Zhou; Rote Paula; Zhang Yanqiao; Nagy Laura E; Wu Jiashin; You Min
Description
An account of the resource
Aberrant precursor mRNA splicing plays a pivotal role in liver diseases. However, roles of splicing regulators in alcoholic liver disease are unknown. Herein, we investigated a splicing regulator, Slu7, in the development of alcoholic steatohepatitis. Adenovirus-mediated alteration of hepatic Slu7 expression in mice pair fed either with or without (as control) ethanol in their diet was used. Knockdown of hepatic Slu7 by adenovirus-Slu7shRNA treatment ameliorated inflammation and attenuated liver injury in mice after ethanol administration. Mechanistically, reducing liver Slu7 expression increased the expression of sirtuin 1 (SIRT1) full-length and repressed the splicing of SIRT1 into
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ajpath.2018.05.004" target="_blank" rel="noreferrer noopener">10.1016/j.ajpath.2018.05.004</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
Department of Pharmaceutical Sciences
Kainrad Noah
Nagy Laura E
NEOMED College of Pharmacy
Rote Paula
Shen Hong
The American journal of pathology
Wang Jiayou
Wu Jiashin
You Min
Zhang Yanqiao
Zhou Zhou
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.ajpath.2016.05.006" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ajpath.2016.05.006</a>
Pages
2417–2428
Issue
9
Volume
186
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
The Detrimental Role Played by Lipocalin-2 in Alcoholic Fatty Liver in Mice.
Publisher
An entity responsible for making the resource available
The American journal of pathology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-09
Subject
The topic of the resource
Alcoholic/*metabolism; Animal; Animals; Blotting; Disease Models; Fatty Liver; Humans; Inbred C57BL; Knockout; Lipocalin-2/*metabolism; Mice; Polymerase Chain Reaction; Western
Creator
An entity primarily responsible for making the resource
Cai Yan; Jogasuria Alvin; Yin Huquan; Xu Ming-Jiang; Hu Xudong; Wang Jiayou; Kim Chunki; Wu Jiashin; Lee Kwangwon; Gao Bin; You Min
Description
An account of the resource
We have previously shown that the ethanol-mediated elevation of lipocaline-2 (LCN2) is closely associated with the development of alcoholic fatty liver disease (AFLD) in mice. Herein, we aimed to understand the functional significance of LCN2 induction by ethanol and to explore its underlying mechanisms. We evaluated the effects of LCN2 in an in vitro cellular alcoholic steatosis model and in an animal study using wild-type and LCN2 knockout mice fed for 4 weeks with an ethanol-supplemented Lieber-DeCarli diet. In the cellular model of alcoholic steatosis, recombinant LCN2 or overexpression of LCN2 exacerbated ethanol-induced fat accumulation, whereas knocking down LCN2 prevented steatosis in hepatocytes exposed to ethanol. Consistently, removal of LCN2 partially but significantly alleviated alcoholic fatty liver injury in mice. Mechanistically, LCN2 mediates detrimental effects of ethanol in the liver via disrupted multiple signaling pathways, including aberrant nicotinamide phosphoribosyltransferase-sirtuin 1 axis, perturbed endocrine metabolic regulatory fibroblast growth factor 15/19 signaling, and impaired chaperone-mediated autophagy. Finally, compared with healthy human livers, liver samples from patients with AFLD had lower gene expression of several
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ajpath.2016.05.006" target="_blank" rel="noreferrer noopener">10.1016/j.ajpath.2016.05.006</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Alcoholic/*metabolism
Animal
Animals
Blotting
Cai Yan
Department of Pharmaceutical Sciences
Disease Models
Fatty Liver
Gao Bin
Hu Xudong
Humans
Inbred C57BL
Jogasuria Alvin
Kim Chunki
Knockout
Lee Kwangwon
Lipocalin-2/*metabolism
Mice
NEOMED College of Pharmacy
Polymerase Chain Reaction
The American journal of pathology
Wang Jiayou
Western
Wu Jiashin
Xu Ming-Jiang
Yin Huquan
You Min
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s11655-016-2621-z" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s11655-016-2621-z</a>
Pages
40–47
Issue
1
Volume
23
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Salvianolate reduces murine myocardial ischemia and reperfusion injury via ERK1/2 signaling pathways in vivo.
Publisher
An entity responsible for making the resource available
Chinese journal of integrative medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-01
Subject
The topic of the resource
*MAP Kinase Signaling System/drug effects; Animal Studies; Animals; Blotting; Cardiotonic Agents/pharmacology/therapeutic use; Chinese medicine; Descriptive Statistics; extracellular signal-regulated kinase 1/2; Flavonoids/pharmacology; Heart Ventricle; Heart Ventricles/drug effects/pathology; In Vivo Studies; Inbred C57BL; ischemia and reperfusion injury; Left; Male; Mice; Mitogen-Activated Protein Kinase 1/*metabolism; Mitogen-Activated Protein Kinase 3/*metabolism; Molecular Structure; Myocardial Ischemia – Drug Therapy; Myocardial Reperfusion Injury – Drug Therapy; Myocardial Reperfusion Injury/*drug therapy/enzymology/pathology; Organ Size/drug effects; P-Value; Phosphorylation; Phosphorylation/drug effects; Plant Extracts – Administration and Dosage; Plant Extracts/chemistry/pharmacology/*therapeutic use; protein kinase B; Protein Kinase Inhibitors – Administration and Dosage; Protein Kinase Inhibitors/pharmacology; Protein Kinases – Analysis; Protein Kinases – Drug Effects; salvianolate; Signal Transduction; Staining and Labeling; Western
Creator
An entity primarily responsible for making the resource
Qi Jianyong; Yu Juan; Huang Dong-Hui; Guo Liheng; Wang Lei; Huang Xin; Huang Hai-Ding; Zhou Miao; Zhang Minzhou; Wu Jiashin
Description
An account of the resource
OBJECTIVE: To analyze the effects of salvianolate on myocardial infarction in a murine in vivo model of ischemia and reperfusion (I/R) injury. METHODS: Myocardial I/R injury model was constructed in mice by 30 min of coronary occlusion followed by 24 h of reperfusion and pretreated with salvianolate 30 min before I/R (SAL group). The SAL group was compared with SHAM (no I/R and no salvianolate), I/R (no salvianolate), and ischemia preconditioning (IPC) groups. Furthermore, an ERK1/2 inhibitor PD98059 (1 mg/kg), and a phosphatidylinositol-3-kinase (PI3-K) inhibitor, LY294002 (7.5 mg/kg), were administered intraperitoneal injection (i.p) for 30 min prior to salvianolate, followed by I/R surgery in LY and PD groups. By using a double staining method, the ratio of the infarct size (IS) to left ventricle (LV) and of risk region (RR) to LV were compared among the groups. Correlations between IS and RR were analyzed. Western-blot was used to detect the extracellular signal-regulated kinase 1/2 (ERK1/2) and protein kinase B (AKT) phosphorylation changes. RESULTS: There were no significant differences between RR to LV ratio among the SHAM, I/R, IPC and SAL groups (P\textgreater0.05). The SAL and IPC groups had IS of 26.1%+/-1.4% and 22.3%+/-2.9% of RR, respectively, both of which were significantly smaller than the I/R group (38.5%+/-2.9% of RR, P\textless0.05, P\textless0.01, respectively). Moreover, the phosphorylation of ERK1/2 was increased in SAL group (P\textless0.05), while AKT had no significant change. LY294002 further reduced IS, whereas the protective role of salvianolate could be attenuated by PD98059, which increased the IS. Additionally, the IS was not linearly related to the RR (r=0.23, 0.45, 0.62, 0.17, and 0.52 in the SHAM, I/R, SAL, LY and PD groups, respectively). CONCLUSION: Salvianolate could reduce myocardial I/R injury in mice in vivo, which involves an ERK1/2 pathway, but not a PI3-K signaling pathway.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s11655-016-2621-z" target="_blank" rel="noreferrer noopener">10.1007/s11655-016-2621-z</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*MAP Kinase Signaling System/drug effects
2017
Animal Studies
Animals
Blotting
Cardiotonic Agents/pharmacology/therapeutic use
Chinese journal of integrative medicine
Chinese medicine
Descriptive Statistics
extracellular signal-regulated kinase 1/2
Flavonoids/pharmacology
Guo Liheng
Heart Ventricle
Heart Ventricles/drug effects/pathology
Huang Dong-Hui
Huang Hai-Ding
Huang Xin
In Vivo Studies
Inbred C57BL
ischemia and reperfusion injury
Left
Male
Mice
Mitogen-Activated Protein Kinase 1/*metabolism
Mitogen-Activated Protein Kinase 3/*metabolism
Molecular Structure
Myocardial Ischemia – Drug Therapy
Myocardial Reperfusion Injury – Drug Therapy
Myocardial Reperfusion Injury/*drug therapy/enzymology/pathology
Organ Size/drug effects
P-Value
Phosphorylation
Phosphorylation/drug effects
Plant Extracts – Administration and Dosage
Plant Extracts/chemistry/pharmacology/*therapeutic use
protein kinase B
Protein Kinase Inhibitors – Administration and Dosage
Protein Kinase Inhibitors/pharmacology
Protein Kinases – Analysis
Protein Kinases – Drug Effects
Qi Jianyong
salvianolate
Signal Transduction
Staining and Labeling
Wang Lei
Western
Wu Jiashin
Yu Juan
Zhang Minzhou
Zhou Miao